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If high levels of glutamic acid are unhealthy, what would be considered a high level?
"Glutamic acid" and "glutamate" are often used interchangeably but, technically, glutamate is the anionic form of glutamic acid. This article doesn't recognize that. RJII 17:01, 9 September 2005 (UTC)
Response to above: whether it exists in the anionic or neutral form is going to be entirely dependent upon the pH - review the Henderson-Hasselbach equation. Cajolingwilhelm 01:30, 14 February 2007 (UTC)
In absence of water it will exist exclusively in the neutral form; and conversion into the glutamate form will always require a chemical reaction, so glutamic acid is the "main" form. Just like HCl is technically called hydrogen chloride and not hydrochloric acid because it won't be the latter unless water or other chemicals are there for it to react with. Glutamic acid is the correct term, but the use of glutamate is indeed extremely common even when it is wrong (and even when people are aware of that fact). It is probably because it is a much more convenient term. Sakkura 03:06, 12 April 2007 (UTC)
Response to above: you are right in that glutamate and glutamic acid are different species, but glutamate is the form taken in most proteins. It will differ with the local chemical environment of the amino acid withing the protein, with the pH at which the organism is living and the ionic strength of the solution. However, in the presence of water, at pH7 (ie in living cells), the amino acid will always predominate in the deprotonated form. Hence, glutamate is the usual physiological form 12:06, 14 August 2007 (GMT)
In the "Pharmacology" section, the following statement is very confusing: "For being so important in the brain functions it is therefore of no surprise that free Glu cannot cross BBB in appreciable quantities; instead it is converted into Glu."
Glu is converted into Glu? I assume that something else was intended.. could somebody clarify? -- Foogod
Glutamine can changed by the enzyme glutamase in glutamatic acid and vice verse. It can also metabolize in y-butter.acid. All this are impotant neurotransmitters in the brain.-- Fackel 21:02, 30 May 2006 (UTC)
Maybe someone mislabeled glutamine as glu? Glu = glutamic acid, gln = glutamine. This mistake is rather common.
Who the hell put up that 3d stereo stick diagram of glutamate? It's completely off. It looks like there's freaking 2 carbons between C1 and C-alpha!!!
What would happen if the the codon were to be deleted all together? What effect would this have on a persons blood cells? could they still carry oxygen? What shape would the cells be?
I need answers, thanks in advance,
Adam
They'd be dead. TimVickers 22:34, 5 January 2007 (UTC)
Not entirely true, it all depends on what that codon is used for and what gene it is deleted from. Some deletions may cause fatality, infact most do. But there are some that may just cause a mutation in the protein which they code for. The protein would obviously have a different 3D shape than what it should, and most likely be digested by proteases. How ever, if the protein is still able to function in some way it will survive. Again it depends on what the codon is for and what gene is involved.
MRCstudent
04:22, 7 February 2007 (UTC)
This article could use at least one reference stating that glutamate does not cross the blood-brain barrier-- if that is in fact the case. That section in general could be more literate; I'd change it myself, but I'd like to know that what I'm proofreading is true first. Well-worded bad info is less likely to attract editorial attention, after all... Kajerm
It is an error, if you beleave that you get a good drive by g. Also the concentration can get enhanced very small. It is the industry for pharmacy, who will tell us such stories. -- Fackel 21:02, 30 May 2006 (UTC)
this article states: "Glutamate easily passes the blood brain barrier:" while the MSG article states "glutamate has a low penetration level in the central nervous system". After reading the linked articles, it seems that it does indeed easily pass through the BBB, but the amount that passes through is regulated. It might be worth noting lest any confusion arise. (hope im not shitting on too many SOPs here. Im new wikipedia) —The preceding unsigned comment was added by 24.16.191.183 ( talk • contribs) .
"There are three glutamate transporters, which belong to the superfamily of transporters that mediate the uptake of GABA, glycine, choline and the biogenic amines. Two of the glutamate transporters appear to be of glial origin, while the third is found in neurons." -- The Biological Basis of Neuropharmacology, 7th ed. (1996) Cooper JR, Bloom FE, Roth RH (*), p 176.
With that in mind: 'Glutamate only crosses the blood-brain barrier when aided by glutamate transporters,' is correct. But the following 'In their absence glutamate begins to build up in the synapse, eventually having an excitotoxic effect' is correct by itself, but contradictory with the previous statement due to proximity. In their absence there is little or no transport across the BBB and so no synaptic build up. If there is enough to support BBB transport, there is enough to handle neuronal (re)uptake and glial uptake. I recommend the second quoted sentence to be amended to 'In their absence, any glutamate already in the intercellular space may build up. An excessive build up can have an excitotoxic effect.'
As far as BBB transmission, "The transport of circulating glutamate to the brain plays only a very minor role in regulating the levels of brain glutamate. In fact, the influx of glutamate from the blood across the [BBB] is much lower than the efflux of glutamate from the brain." (* ibid, p 171). The lack of that efflux (due to low levels of transporters) is at least one of the neurotoxic mechanisms, as "...glutamate plays an important function in the detoxicification of ammonia in the brain..." (* ibid, p 171).
-- Drmcclainphd 06:35, 27 June 2006 (UTC)drmcclainphd (at gmail), an actual neuroscientist
I can't find the "low penetration" quote mentioned in the original question in the MSG article anymore, and an (admittedly, fairly quick) scan of both articles doesn't look like there's any significant contradiction on this subject, as far as I can see. Perhaps the contradiction tag should be removed? -- Foogod 18:44, 13 April 2007 (UTC)
the article notes: "In particular Glutamate Restriction Diets are now claiming success anecdotally, by limiting or eliminating intake of wheat, peanut, soy and bean. No similar diets for Schizophrenia are known." I'm going to lower-case schizophrenia, but my question is, if this sentence is to remain, should there be reference to Abram Hoffer and Humphrey Osmund's research in niacinamide (B3) therapies?? [1] Their chemistry is sound but many people have attacked their double-blind studies. My first thought is not to mention these dudes as this article has very little to do with schizophrenia and perhaps the last sentence should be taken out entirely (it's certainly not true, if the B3 diet does in fact help some kinds of schizophrenics). Before I do anything, I'd like to see thoughts, comments. Gaviidae 11:03, 22 June 2006 (UTC)
My thoughs are that schizophrenia seems to be off topic. Certainly, glutamate has something going on with the brain. I have anecdotal information also, but the wiki is not for that. It should be solid and concrete. There is a policy on avoiding "creeping words". This article, if not listed as such, should be. It has problems. The topic of B3 should also be avoided. Anti-MSG point to a B-6 deficency as a probable cause for MSG intolerance.
In any case, if something is mention, it should have a direct relationship. Unless, of course, it can be shown why an indirect relationship clearly needs to be mentioned.
-- meatclerk 04:33, 23 June 2006 (UTC)
Definitely dump the schizophrenia and diet text. In the brain, glutamate is released at 9/10 fast synapses between cells (as assessed by anatomy). So it gets mentioned in the context of all brain diseases. But as far as I'm concerned, these ideas are not important or verifiable in this context. Aplested 00:03, 28 August 2006 (UTC)
As I seem to have recovered, albeit slowly, from the disease in question, I feel torn not to add something about using brewer's yeast as a source of glutamic acid, which has been indispensable.
Educationandbuilding
04:25, 3 August 2007 (UTC)
Of interest might be a recently controlled-release drug treatment for schizophrenia, tentatively called LY2140023, which acts as a glutamate receptor agonist. More information at
[2].
Batula
05:45, 12 September 2007 (UTC)
I made a number of changes to this section, added a reference for caged analog. I reduced the section about the nanosensor. This is a neat idea, but the sensor doesn't work for the purpose it was quoted. It is probably too slow for anything with a synapse. It didn't make sense for this to be such a big section. I tried to cut out repetition and move the section closer to the consensus views, and away from guesses. I'm not sure about the epilepsy section, it is plausible but is not referenced properly. This is more of a technique for getting an animal model of epilepsy in my view, which is much more complicated than simple lots of glu. That's more like a stroke. It could be interesting to add some brief history about how glutamate came to be accepted as a neurotransmitter after a 30 year struggle - that is, the development of antagonists. Aplested 02:14, 28 August 2006 (UTC)
I added a paragraph on invertebrates, particularly nematodes and arthropods, where glutamate is an inhibitory neurotransmitter, acting on glu-gated chloride channels. This receptor has important pharmacological implications, being the target for avermectins, important antiparasitic agents in veterinary and human medicine.
Is it not the case that NDMA receptors require activation of the post-synaptic neuron (that is, the neuron to which they are affixed on the dendrite) in order to expel a magnesium ion and allow functionality of glutamate as an NDMA receptor agonist? If so, that should be noted and sourced in this article. RadicalHarmony ( talk) 07:31, 22 December 2007 (UTC)
This is an important question that nobody seems to be answering, or able to answer. Many people think it's the same thing, including companies of protein powders that think the names "L-Glutamine" and "Glutamic Acid" are interchangeable. We need this correctly addressed once and for all. —Preceding unsigned comment added by 174.18.81.22 ( talk) 20:10, 14 July 2009 (UTC)
please add this to the picture. Thanks!! 76.174.42.22 ( talk) 04:17, 17 June 2008 (UTC)
This article talk page was automatically added with {{ WikiProject Food and drink}} banner as it falls under Category:Food or one of its subcategories. If you find this addition an error, Kindly undo the changes and update the inappropriate categories if needed. The bot was instructed to tagg these articles upon consenus from WikiProject Food and drink. You can find the related request for tagging here . Maximum and carefull attention was done to avoid any wrongly tagging any categories , but mistakes may happen... If you have concerns , please inform on the project talk page -- TinucherianBot ( talk) 17:31, 3 July 2008 (UTC)
Can someone please check the external link from the sentence "Some protein-rich plant foods also serve as sources."? I'm not sure, but I don't see anything on the reference site talking about plant foods, and instead seems to be indirectly selling "nutrition supplements".
-- Hellsop ( talk) 14:35, 15 September 2008 (UTC)
Under "History" the article says "This compound was discovered in 1908 by the professor Kikunae Ikeda" but:
peptideguide.com says "Glutamic acid is a non-essential amino acid, was first isolated from wheat gluten in 1866 by the German chemist Karl Ritthausen. The chemical structure of the amino acid was identified in 1890." at http://www.peptideguide.com/amino-acids/glutamic-acid.html
medterms.com states it was isolated from wheat gluten in 1866: http://www.medterms.com/script/main/art.asp?articlekey=22824
As does this article published in 1948: http://blog.modernmechanix.com/2007/09/08/pills-that-increase-your-intelligence/
While the current "History" section is interesting, it would seem that it's a particular chapter in the history of glutamic acid regarding taste, seaweed and oriental food. But it currently reads as if glutamic's history starts at 1908.
ChuckEsterbrook ( talk) 06:40, 25 November 2008 (UTC)
The term "Free Glutamic Acid" is used only once in the entire article and it is used "in passing". The average reader could not infer the meaning of the qualifier "Free" in this context. Could someone with knowledge on the subject (not me) explain the meaning of "Free Glutamic Acid" vs "Glutamic Acid"? Thanks. Travis28 ( talk) 21:58, 29 November 2011 (UTC)
Suggestion: add information on food sources
Suggestion: add information on deficiency reasons and symptoms.
What's the molecular formula?
Eg:
Phenylalanine has a chemical formula of C9H11NO2 but a molecular forumla of C6H5CH2CHCOOH
~ender 2014-10-05 3:13:AM MST — Preceding
unsigned comment added by
71.223.87.212 (
talk •
contribs)
10:15, 5 October 2014 (UTC)
I'd like to note that today I created glutamate (neurotransmitter), initializing it by copying and pasting the contents of the "Neurotransmitter" section of this article. I have added a "main" link; over the coming days I plan to simplify the contents of that section to avoid duplication. I think perhaps it would also be good to add some dab info at the top of this article, but I won't do that immediately. Looie496 ( talk) 14:25, 3 December 2015 (UTC)
The comment(s) below were originally left at Talk:Glutamic acid/Comments, and are posted here for posterity. Following several discussions in past years, these subpages are now deprecated. The comments may be irrelevant or outdated; if so, please feel free to remove this section.
I am not aware of designations of Glx or Z for the glutamic acid. Also, glutamic acid (Glu or E) and glutamine (Gln or Q) are different, although related amino acids. |
Last edited at 22:31, 17 February 2008 (UTC). Substituted at 16:25, 29 April 2016 (UTC)
The reference for glutamate not readily passing the blood brain barrier was tagged as possibly being an unreliable source because supplements to
The Journal of Nutrition might not be peer reviewed, but as can be seen
here, they are: " After submission to the editorial office, the Journal editor will appoint a Supplement Editor and all supplement manuscripts will undergo peer review."
I've added another reference to a supplement of
The American Journal of Clinical Nutrition, which is
also peer reviewed: "The second step involves anonymous peer review of the individual articles."
and ...will be reviewed according to the same scientific standards used to evaluate original research articles."
--
tronvillain (
talk)
20:23, 25 July 2016 (UTC)
I have moved this talk topic to the Monosodium glutamate talk page, since it seems more appropriate there. --( talk) 21:56, 4 October 2017 (UTC)
The first link doesn't lead to the article - proper link is https://academic.oup.com/jn/article/130/4/1016S/4686663?searchresult=1
The article says "Glutamic acid can exist in three optical isomers, including the dextrorotatory L-form, d(−), and l(+)".
Surely that should be two optical isomers, namely the dextrorotatory L-form or L(+) form and the levorotatory D-form or D(−) ? The quoted source for the claim that there are three is Webster's Third New International Dictionary of the English Language, which doesn't sound like the best source of chemistry information to me.
-- HairyDan ( talk) 11:00, 21 December 2021 (UTC)
^ I just noticed the same thing and have 100% the same response. I came strait to the talk page and found someone had already noticed the same problem so I would like to double down on their response. There is only one stereocenter so there can only be two possible optical isomers. Whoever initially wrote this section might have been confused by the separate notations for the same stereoisomeric designation: "dextrorotary" = "+" and "levorotary" = "−" so the author's listing of L(+) as an optical state is innately contradictory. It is equivalent to saying "there are three directions you car can turn in: a left turn, a right turn, and a leftright turn." 162.220.42.222 ( talk) 21:40, 23 February 2022 (UTC)
This is the
talk page for discussing improvements to the
Glutamic acid article. This is not a forum for general discussion of the article's subject. |
Article policies
|
Find sources: Google ( books · news · scholar · free images · WP refs) · FENS · JSTOR · TWL |
This
level-5 vital article is rated C-class on Wikipedia's
content assessment scale. It is of interest to the following WikiProjects: | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
|
If high levels of glutamic acid are unhealthy, what would be considered a high level?
"Glutamic acid" and "glutamate" are often used interchangeably but, technically, glutamate is the anionic form of glutamic acid. This article doesn't recognize that. RJII 17:01, 9 September 2005 (UTC)
Response to above: whether it exists in the anionic or neutral form is going to be entirely dependent upon the pH - review the Henderson-Hasselbach equation. Cajolingwilhelm 01:30, 14 February 2007 (UTC)
In absence of water it will exist exclusively in the neutral form; and conversion into the glutamate form will always require a chemical reaction, so glutamic acid is the "main" form. Just like HCl is technically called hydrogen chloride and not hydrochloric acid because it won't be the latter unless water or other chemicals are there for it to react with. Glutamic acid is the correct term, but the use of glutamate is indeed extremely common even when it is wrong (and even when people are aware of that fact). It is probably because it is a much more convenient term. Sakkura 03:06, 12 April 2007 (UTC)
Response to above: you are right in that glutamate and glutamic acid are different species, but glutamate is the form taken in most proteins. It will differ with the local chemical environment of the amino acid withing the protein, with the pH at which the organism is living and the ionic strength of the solution. However, in the presence of water, at pH7 (ie in living cells), the amino acid will always predominate in the deprotonated form. Hence, glutamate is the usual physiological form 12:06, 14 August 2007 (GMT)
In the "Pharmacology" section, the following statement is very confusing: "For being so important in the brain functions it is therefore of no surprise that free Glu cannot cross BBB in appreciable quantities; instead it is converted into Glu."
Glu is converted into Glu? I assume that something else was intended.. could somebody clarify? -- Foogod
Glutamine can changed by the enzyme glutamase in glutamatic acid and vice verse. It can also metabolize in y-butter.acid. All this are impotant neurotransmitters in the brain.-- Fackel 21:02, 30 May 2006 (UTC)
Maybe someone mislabeled glutamine as glu? Glu = glutamic acid, gln = glutamine. This mistake is rather common.
Who the hell put up that 3d stereo stick diagram of glutamate? It's completely off. It looks like there's freaking 2 carbons between C1 and C-alpha!!!
What would happen if the the codon were to be deleted all together? What effect would this have on a persons blood cells? could they still carry oxygen? What shape would the cells be?
I need answers, thanks in advance,
Adam
They'd be dead. TimVickers 22:34, 5 January 2007 (UTC)
Not entirely true, it all depends on what that codon is used for and what gene it is deleted from. Some deletions may cause fatality, infact most do. But there are some that may just cause a mutation in the protein which they code for. The protein would obviously have a different 3D shape than what it should, and most likely be digested by proteases. How ever, if the protein is still able to function in some way it will survive. Again it depends on what the codon is for and what gene is involved.
MRCstudent
04:22, 7 February 2007 (UTC)
This article could use at least one reference stating that glutamate does not cross the blood-brain barrier-- if that is in fact the case. That section in general could be more literate; I'd change it myself, but I'd like to know that what I'm proofreading is true first. Well-worded bad info is less likely to attract editorial attention, after all... Kajerm
It is an error, if you beleave that you get a good drive by g. Also the concentration can get enhanced very small. It is the industry for pharmacy, who will tell us such stories. -- Fackel 21:02, 30 May 2006 (UTC)
this article states: "Glutamate easily passes the blood brain barrier:" while the MSG article states "glutamate has a low penetration level in the central nervous system". After reading the linked articles, it seems that it does indeed easily pass through the BBB, but the amount that passes through is regulated. It might be worth noting lest any confusion arise. (hope im not shitting on too many SOPs here. Im new wikipedia) —The preceding unsigned comment was added by 24.16.191.183 ( talk • contribs) .
"There are three glutamate transporters, which belong to the superfamily of transporters that mediate the uptake of GABA, glycine, choline and the biogenic amines. Two of the glutamate transporters appear to be of glial origin, while the third is found in neurons." -- The Biological Basis of Neuropharmacology, 7th ed. (1996) Cooper JR, Bloom FE, Roth RH (*), p 176.
With that in mind: 'Glutamate only crosses the blood-brain barrier when aided by glutamate transporters,' is correct. But the following 'In their absence glutamate begins to build up in the synapse, eventually having an excitotoxic effect' is correct by itself, but contradictory with the previous statement due to proximity. In their absence there is little or no transport across the BBB and so no synaptic build up. If there is enough to support BBB transport, there is enough to handle neuronal (re)uptake and glial uptake. I recommend the second quoted sentence to be amended to 'In their absence, any glutamate already in the intercellular space may build up. An excessive build up can have an excitotoxic effect.'
As far as BBB transmission, "The transport of circulating glutamate to the brain plays only a very minor role in regulating the levels of brain glutamate. In fact, the influx of glutamate from the blood across the [BBB] is much lower than the efflux of glutamate from the brain." (* ibid, p 171). The lack of that efflux (due to low levels of transporters) is at least one of the neurotoxic mechanisms, as "...glutamate plays an important function in the detoxicification of ammonia in the brain..." (* ibid, p 171).
-- Drmcclainphd 06:35, 27 June 2006 (UTC)drmcclainphd (at gmail), an actual neuroscientist
I can't find the "low penetration" quote mentioned in the original question in the MSG article anymore, and an (admittedly, fairly quick) scan of both articles doesn't look like there's any significant contradiction on this subject, as far as I can see. Perhaps the contradiction tag should be removed? -- Foogod 18:44, 13 April 2007 (UTC)
the article notes: "In particular Glutamate Restriction Diets are now claiming success anecdotally, by limiting or eliminating intake of wheat, peanut, soy and bean. No similar diets for Schizophrenia are known." I'm going to lower-case schizophrenia, but my question is, if this sentence is to remain, should there be reference to Abram Hoffer and Humphrey Osmund's research in niacinamide (B3) therapies?? [1] Their chemistry is sound but many people have attacked their double-blind studies. My first thought is not to mention these dudes as this article has very little to do with schizophrenia and perhaps the last sentence should be taken out entirely (it's certainly not true, if the B3 diet does in fact help some kinds of schizophrenics). Before I do anything, I'd like to see thoughts, comments. Gaviidae 11:03, 22 June 2006 (UTC)
My thoughs are that schizophrenia seems to be off topic. Certainly, glutamate has something going on with the brain. I have anecdotal information also, but the wiki is not for that. It should be solid and concrete. There is a policy on avoiding "creeping words". This article, if not listed as such, should be. It has problems. The topic of B3 should also be avoided. Anti-MSG point to a B-6 deficency as a probable cause for MSG intolerance.
In any case, if something is mention, it should have a direct relationship. Unless, of course, it can be shown why an indirect relationship clearly needs to be mentioned.
-- meatclerk 04:33, 23 June 2006 (UTC)
Definitely dump the schizophrenia and diet text. In the brain, glutamate is released at 9/10 fast synapses between cells (as assessed by anatomy). So it gets mentioned in the context of all brain diseases. But as far as I'm concerned, these ideas are not important or verifiable in this context. Aplested 00:03, 28 August 2006 (UTC)
As I seem to have recovered, albeit slowly, from the disease in question, I feel torn not to add something about using brewer's yeast as a source of glutamic acid, which has been indispensable.
Educationandbuilding
04:25, 3 August 2007 (UTC)
Of interest might be a recently controlled-release drug treatment for schizophrenia, tentatively called LY2140023, which acts as a glutamate receptor agonist. More information at
[2].
Batula
05:45, 12 September 2007 (UTC)
I made a number of changes to this section, added a reference for caged analog. I reduced the section about the nanosensor. This is a neat idea, but the sensor doesn't work for the purpose it was quoted. It is probably too slow for anything with a synapse. It didn't make sense for this to be such a big section. I tried to cut out repetition and move the section closer to the consensus views, and away from guesses. I'm not sure about the epilepsy section, it is plausible but is not referenced properly. This is more of a technique for getting an animal model of epilepsy in my view, which is much more complicated than simple lots of glu. That's more like a stroke. It could be interesting to add some brief history about how glutamate came to be accepted as a neurotransmitter after a 30 year struggle - that is, the development of antagonists. Aplested 02:14, 28 August 2006 (UTC)
I added a paragraph on invertebrates, particularly nematodes and arthropods, where glutamate is an inhibitory neurotransmitter, acting on glu-gated chloride channels. This receptor has important pharmacological implications, being the target for avermectins, important antiparasitic agents in veterinary and human medicine.
Is it not the case that NDMA receptors require activation of the post-synaptic neuron (that is, the neuron to which they are affixed on the dendrite) in order to expel a magnesium ion and allow functionality of glutamate as an NDMA receptor agonist? If so, that should be noted and sourced in this article. RadicalHarmony ( talk) 07:31, 22 December 2007 (UTC)
This is an important question that nobody seems to be answering, or able to answer. Many people think it's the same thing, including companies of protein powders that think the names "L-Glutamine" and "Glutamic Acid" are interchangeable. We need this correctly addressed once and for all. —Preceding unsigned comment added by 174.18.81.22 ( talk) 20:10, 14 July 2009 (UTC)
please add this to the picture. Thanks!! 76.174.42.22 ( talk) 04:17, 17 June 2008 (UTC)
This article talk page was automatically added with {{ WikiProject Food and drink}} banner as it falls under Category:Food or one of its subcategories. If you find this addition an error, Kindly undo the changes and update the inappropriate categories if needed. The bot was instructed to tagg these articles upon consenus from WikiProject Food and drink. You can find the related request for tagging here . Maximum and carefull attention was done to avoid any wrongly tagging any categories , but mistakes may happen... If you have concerns , please inform on the project talk page -- TinucherianBot ( talk) 17:31, 3 July 2008 (UTC)
Can someone please check the external link from the sentence "Some protein-rich plant foods also serve as sources."? I'm not sure, but I don't see anything on the reference site talking about plant foods, and instead seems to be indirectly selling "nutrition supplements".
-- Hellsop ( talk) 14:35, 15 September 2008 (UTC)
Under "History" the article says "This compound was discovered in 1908 by the professor Kikunae Ikeda" but:
peptideguide.com says "Glutamic acid is a non-essential amino acid, was first isolated from wheat gluten in 1866 by the German chemist Karl Ritthausen. The chemical structure of the amino acid was identified in 1890." at http://www.peptideguide.com/amino-acids/glutamic-acid.html
medterms.com states it was isolated from wheat gluten in 1866: http://www.medterms.com/script/main/art.asp?articlekey=22824
As does this article published in 1948: http://blog.modernmechanix.com/2007/09/08/pills-that-increase-your-intelligence/
While the current "History" section is interesting, it would seem that it's a particular chapter in the history of glutamic acid regarding taste, seaweed and oriental food. But it currently reads as if glutamic's history starts at 1908.
ChuckEsterbrook ( talk) 06:40, 25 November 2008 (UTC)
The term "Free Glutamic Acid" is used only once in the entire article and it is used "in passing". The average reader could not infer the meaning of the qualifier "Free" in this context. Could someone with knowledge on the subject (not me) explain the meaning of "Free Glutamic Acid" vs "Glutamic Acid"? Thanks. Travis28 ( talk) 21:58, 29 November 2011 (UTC)
Suggestion: add information on food sources
Suggestion: add information on deficiency reasons and symptoms.
What's the molecular formula?
Eg:
Phenylalanine has a chemical formula of C9H11NO2 but a molecular forumla of C6H5CH2CHCOOH
~ender 2014-10-05 3:13:AM MST — Preceding
unsigned comment added by
71.223.87.212 (
talk •
contribs)
10:15, 5 October 2014 (UTC)
I'd like to note that today I created glutamate (neurotransmitter), initializing it by copying and pasting the contents of the "Neurotransmitter" section of this article. I have added a "main" link; over the coming days I plan to simplify the contents of that section to avoid duplication. I think perhaps it would also be good to add some dab info at the top of this article, but I won't do that immediately. Looie496 ( talk) 14:25, 3 December 2015 (UTC)
The comment(s) below were originally left at Talk:Glutamic acid/Comments, and are posted here for posterity. Following several discussions in past years, these subpages are now deprecated. The comments may be irrelevant or outdated; if so, please feel free to remove this section.
I am not aware of designations of Glx or Z for the glutamic acid. Also, glutamic acid (Glu or E) and glutamine (Gln or Q) are different, although related amino acids. |
Last edited at 22:31, 17 February 2008 (UTC). Substituted at 16:25, 29 April 2016 (UTC)
The reference for glutamate not readily passing the blood brain barrier was tagged as possibly being an unreliable source because supplements to
The Journal of Nutrition might not be peer reviewed, but as can be seen
here, they are: " After submission to the editorial office, the Journal editor will appoint a Supplement Editor and all supplement manuscripts will undergo peer review."
I've added another reference to a supplement of
The American Journal of Clinical Nutrition, which is
also peer reviewed: "The second step involves anonymous peer review of the individual articles."
and ...will be reviewed according to the same scientific standards used to evaluate original research articles."
--
tronvillain (
talk)
20:23, 25 July 2016 (UTC)
I have moved this talk topic to the Monosodium glutamate talk page, since it seems more appropriate there. --( talk) 21:56, 4 October 2017 (UTC)
The first link doesn't lead to the article - proper link is https://academic.oup.com/jn/article/130/4/1016S/4686663?searchresult=1
The article says "Glutamic acid can exist in three optical isomers, including the dextrorotatory L-form, d(−), and l(+)".
Surely that should be two optical isomers, namely the dextrorotatory L-form or L(+) form and the levorotatory D-form or D(−) ? The quoted source for the claim that there are three is Webster's Third New International Dictionary of the English Language, which doesn't sound like the best source of chemistry information to me.
-- HairyDan ( talk) 11:00, 21 December 2021 (UTC)
^ I just noticed the same thing and have 100% the same response. I came strait to the talk page and found someone had already noticed the same problem so I would like to double down on their response. There is only one stereocenter so there can only be two possible optical isomers. Whoever initially wrote this section might have been confused by the separate notations for the same stereoisomeric designation: "dextrorotary" = "+" and "levorotary" = "−" so the author's listing of L(+) as an optical state is innately contradictory. It is equivalent to saying "there are three directions you car can turn in: a left turn, a right turn, and a leftright turn." 162.220.42.222 ( talk) 21:40, 23 February 2022 (UTC)